| http://purl.uniprot.org/citations/17681938 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17681938 | http://www.w3.org/2000/01/rdf-schema#comment | "Induction of heme oxygenase-1 (HO-1) expression has been associated with adaptive cytoprotection against a wide array of toxic insults, but the underlying molecular mechanisms remain largely unresolved. In this study, we investigated the potential role of carbon monoxide (CO), one of the by-products of the HO-1 reaction, in the adaptive survival response to peroxynitrite-induced PC12 cell death. Upon treatment of rat pheochromocytoma (PC12) cells with the peroxynitrite generator 3-morpholinosydnonimine hydrochloride (SIN-1), the cellular GSH level decreased initially, but was gradually restored to the basal level. This was accompanied by increased expression of the catalytic subunit of glutamate-cysteine ligase (GCLC), the rate-limiting enzyme in GSH biosynthesis. The SIN-1-induced GCLC up-regulation was preceded by induction of HO-1 and subsequent CO production. Inhibition of HO activity by zinc protoporphyrin IX or knockdown of HO-1 gene expression by small interfering RNA abrogated the up-regulation of GCLC expression and the subsequent GSH restoration induced by SIN-1. In contrast, additional exposure to the CO-releasing molecule (CO-RM) restored the GSH level previously reduced by inhibition of CO production using zinc protoporphyrin IX. Furthermore, CO-RM treatment up-regulated GCLC expression through activation of Nrf2. The CO-RM-induced activation of Nrf2 was under the control of the phosphatidylinositol 3-kinase/Akt signaling pathway. In conclusion, CO produced by HO-1 rescues PC12 cells from nitrosative stress through induction of GCLC, which is mediated by activation of phosphatidylinositol 3-kinase/Akt and subsequently Nrf2 signaling."xsd:string |
| http://purl.uniprot.org/citations/17681938 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m701916200"xsd:string |
| http://purl.uniprot.org/citations/17681938 | http://purl.uniprot.org/core/author | "Li M.H."xsd:string |
| http://purl.uniprot.org/citations/17681938 | http://purl.uniprot.org/core/author | "Jang J.H."xsd:string |
| http://purl.uniprot.org/citations/17681938 | http://purl.uniprot.org/core/author | "Cha Y.N."xsd:string |
| http://purl.uniprot.org/citations/17681938 | http://purl.uniprot.org/core/author | "Na H.K."xsd:string |
| http://purl.uniprot.org/citations/17681938 | http://purl.uniprot.org/core/author | "Surh Y.J."xsd:string |
| http://purl.uniprot.org/citations/17681938 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
| http://purl.uniprot.org/citations/17681938 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
| http://purl.uniprot.org/citations/17681938 | http://purl.uniprot.org/core/pages | "28577-28586"xsd:string |
| http://purl.uniprot.org/citations/17681938 | http://purl.uniprot.org/core/title | "Carbon monoxide produced by heme oxygenase-1 in response to nitrosative stress induces expression of glutamate-cysteine ligase in PC12 cells via activation of phosphatidylinositol 3-kinase and Nrf2 signaling."xsd:string |
| http://purl.uniprot.org/citations/17681938 | http://purl.uniprot.org/core/volume | "282"xsd:string |
| http://purl.uniprot.org/citations/17681938 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/17681938 |
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